In this next year we propose to study the alterations in pulmonary metabolic function both in-vitro as well as in animals and man, under conditions of acute non-hydrostatic pulmonary edema as well as positive end expiratory pressure. Specifically we will examine plasma for the presence of negative inotropic agents, for agents that alter red cell glycolytic pathways and for the presence of materials that stimulate the fibrinolytic system. Finally we will continue to evaluate the pulmonary endothelial clearance of serotonin during pressure breathing.